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Muscle-fiber loss is a characteristic of many progressive neuromuscular disorders. Over the past decade, identification of a growing number of apoptosis-associated factors and events in pathological skeletal muscle provided increasing evidence that apoptotic cell-death mechanisms account significantly for muscle-fiber atrophy and loss in a wide spectrum of neuromuscular disorders. It became obvious that there is not one specific pathway for muscle fibers to undergo apoptotic degradation. In contrast, certain neuromuscular diseases seem to involve characteristic expression patterns of apoptosis-related factors and pathways. Furthermore, there are some characteristics of muscle-fiber apoptosis that rely on the muscle fiber itself as an extremely specified cell type. Multinucleated muscle fibers with successive muscle-fiber segments controlled by individual nuclei display some specifics different from apoptosis of mononucleated cells. This review focuses on the expression patterns of apoptosis-associated factors in different primary and secondary neuromuscular disorders and gives a synopsis of current knowledge.

In tumor tissue specimens of 27 primary and 17 secondary glioblastomas and the precursor lesions, the immunohistochemical expression patterns of the membrane protein CD44s, the basal lamina proteins laminin, collagen IV, and fibronectin, the lectin galectin-3 recognizing tenascin and N-CAM as well as of the matrix-degrading enzymes matrix metalloproteinase MMP-2 and MMP-9, and cathepsin D were studied. Besides expression of basal lamina proteins in vessels, all glioblastomas and the precursor lesions showed strong immunoreactivity of CD44s, tenascin, galectin-3, and N-CAM which were restricted to solid tumor masses. Present in solid tumor areas, MMP-2, MMP-9 and cathepsin D were also strongly expressed by single tumors cells invading adjacent brain tissue at the infiltrative margin. Neither the expression pattern in primary and secondary glioblastomas nor in the precursor tumors revealed significant differences. There was also no intraindividual constant expression pattern during glioma progression or correlation with malignancy. Restricted expression of CD44s, galectin-3, tenascin and N-CAM in solid tumor masses seems to contribute to homotypic tumor cell adhesion while single tumor cells abolish this expression profile and acquire invasive activities by expression of cathepsin D, MMP-2 and MMP-9.

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